title: Correlation between extent of myocardial dysfunction and markers of irreversible damage in failing hearts.
abstract: BACKGROUND
  The structural correlates of 201Tl uptake in patients with advanced postischemic pump dysfunction are unclear. There are no good experimental models adequately reflecting the mixture of normal, dysfunctional but viable, and necrotic regions characteristic of chronic ischemic heart disease in human beings.
  
  
  RESULTS
  Four heart transplant candidates with idiopathic dilated cardiomyopathy and seven with ischemic heart disease underwent rest-injection 4-hour redistribution 201Tl single-photon emission computed tomography before surgery. Delayed tracer uptake was categorized into severely reduced (<50%), mildly or moderately reduced (50% to 74%), and normal (> or =75%) and related to echocardiographic wall motion and histologic findings in the hearts excised at transplantation. In idiopathic dilated cardiomyopathy, despite severe wall motion impairment, minimal or mild myocardial damage and homogeneously high 201Tl uptake were found. In ischemic heart disease, wall motion did not discriminate extensive from mild structural damage. 201Tl activity was inversely related to myocardial fibrosis (r = -0.50, p = 0.0001). Severe defects in 201Tl uptake (<50%) predicted extensive (>30%) fibrosis with 83% sensitivity and 63% specificity. Segmental akinesis and apical location resulted in loss of sensitivity (74% and 58%, respectively). No histologic or wall motion abnormality accounted for poor specificity. In the individual patient, more than nine segments determined viable by imaging criteria predicted left ventricular fibrosis of less than 15% with 86% accuracy.
  
  
  CONCLUSIONS
  This histopathologic-clinical correlative study supports current evidence of good sensitivity but limited specificity of 201Tl rest-redistribution tomographic imaging in the evaluation of viable myocardium. In the individual patient, more than nine viable segments reliably predicted a limited extension of fibrosis.
authors.affiliation: C.N.R. Clinical Physiology Institute, Section of Milan, Niguarda Hospital, Italy.
authors.forename: R
authors.initials: R
authors.lastname: De Maria
authors.forename: L
authors.initials: L
authors.lastname: Ruffini
authors.forename: R
authors.initials: R
authors.lastname: Testa
authors.forename: M
authors.initials: M
authors.lastname: Parolini
authors.forename: M
authors.initials: M
authors.lastname: Mangiavacchi
authors.forename: E
authors.initials: E
authors.lastname: Vitali
authors.forename: M
authors.initials: M
authors.lastname: Merli
authors.forename: G
authors.initials: G
authors.lastname: Sambuceti
authors.forename: A
authors.initials: A
authors.lastname: Pellegrini
authors.forename: G
authors.initials: G
authors.lastname: Baroldi
authors.forename: O
authors.initials: O
authors.lastname: Parodi
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D006321:Heart / Q000000981:diagnostic imaging*; D016027:Heart Transplantation; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D011877:Radionuclide Imaging; D013794:Thallium Radioisotopes; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology
chemical_list: D013794:Thallium Radioisotopes